GeneWatch PR: Google's gene test company 23andMe proves its own business is useless

Online gene testing company 23andMe this week
published its first genetic research study into Parkinson's Disease. The study
was funded by the participants (many of whom are customers of 23andMe), the
company itself, and Google-founder Sergei Brin, who is married to 23andMe's CEO
and founder, Anne Wojcicki. Wojcicki is also personally subsidising the failing
company and is a co-author on the paper (1).

23andMe's study shows that two new genes it has
discovered, plus all known existing genes linked to the disease, are not much
better than random selection at predicting who will get Parkinson's Disease.

Google's electronic medical record service Google
Health has also been a business failure and was wound up this week.

According to the new research, predictive computer
models including all known genes can only account for 6%-7% of the variance of
the disease (2). This means that 93-94% of the explanation for differences in
people's likelihood of developing Parkinson's Disease is missing. Further, most
of the missing explanation for these differences in risk is not genetic.

"Most diseases in most people are not predictable from people's genes," said Dr Helen Wallace "23andMe should start being more honest with
its customers and admit most gene tests that it sells online are meaningless.
Both its investors and its customers need to know that genetic predictions will
always have fundamental limitations. These findings show that 23andMe's product
can only ever get a little bit less useless as more and more research is done."

23andMe's rival company, DeCode Genetics (based in Iceland)
went bankrupt in 2009, although it continues to operate as a private company
(3). A recent study presented at the European Society of Human Genetics concluded
that both companies sell
inaccurate predictions of disease risks to their customers
(4).

23andMe's paper includes a new estimate that the heritability
of Parkinson's Disease is 23% (suggesting that 77% of the variance will never
be explained by genes, but that missing genes yet to be discovered account for
a further 16%). Even if this (rather high) estimate is correct, it is much less
than the calculated heritability of type 1 diabetes, a disease for which
scientists have already shown genetic tests will have poor predictive value
(5). The authors of the paper predict that even if all the genes they think
might exist were found there would be an upper bound on the predictive value
which is insufficient to make genetic screening for Parkinson's Disease risk useful
in the general population (6). In short, this means its tests will never be
useful to its customers. In addition, only 17 of 42 previously reported links
between genes and Parkinson's Disease were replicated in the paper,
highlighting ongoing statistical problems with this type of study.

GeneWatch has previously criticised 23andMe and other
companies for wrongly implying that genetic differences play a major role in
determining who develops Parkinson's Disease and other common diseases, and
ignoring environmental factors (7). Although environmental risks - including
smoking, diets and pollution - are sometimes also small, they can be reduced,
unlike a person's genes which can't be changed.

"The big
difference between genetic and environmental factors is that reduced exposure
to unhealthy products or pollution can make a massive difference to the number
of cases of disease" said Dr Wallace. "However,
there are lots of vested interests that prefer researchers to be focused on the
supposed risk of people's genes".

The idea that genetic screening would allow scientists
to predict who would develop common diseases such as cancer was originally
developed by the eugenicists who went to work for the tobacco industry in the
1950s. The false tobacco industry claims were endorsed by leading geneticists
in the run up to the Human Genome Project in order to obtain funding for the
project (8). The food, nuclear and chemical industries also poured money into
genetic research (9). They sought to blame genes, rather than their own
products or pollution, for cancer, hypertension, obesity and diabetes (10). The
pharmaceutical industry expected to massively expand the drug market by selling
medicines to healthy people told that they are at high genetic risk.

"Google should
have studied the history of misleading claims about genetics and disease before
setting up this company" said Dr Wallace. "Maybe next time they will sponsor a more useful study into the role of
pesticides in Parkinson's Disease".

Identifying genes that play a role in common diseases
can help scientists to understand the biology of a disease, but this does not
mean that tests of these genes are useful to predict who will get a disease or
to decide who should change their lifestyle or take medication. Gene tests are
nevertheless useful to diagnose rare genetic disorders and rare familial forms
of common disorders in high-risk families.

(2)Sergei Brin himself has a rare gene
linked with a rare familial (i.e. largely inherited) form of Parkinson's
Disease which occurs mainly in Jewish families. However, most cases of
Parkinson's disease are not familial.

(5)Clayton, DG (2009) Prediction and Interaction in
Complex Disease Genetics:Experience in Type 1 Diabetes. PLoS Genetics, 5(7): e1000540. On: http://www.plosgenetics.org/article/info:doi/10.1371/journal.pgen.1000540
"Many authors have recently commented on the modest
predictive power of the common disease susceptability loci currently emerging.
However, here it is suggested that, for most diseases, this would remain the
case even if all relevant loci (including rare variants) were ultimately
discovered."

(6)They
report an AUC for their own model of 0.55 to 0.6 and an "upper bound on AUC for a genetic risk prediction model of 0.83 to 0.88"
(based on finding future genes to explain their calculated heritability). An
AUC of 1 implies perfect predictions, an AUC of 0.5 is no better than random
guessing. It has been suggested elsewhere that an AUC of 0.75 is needed before
testing people with symptoms and an AUC of 0.99 for screening unsymptomatic
people in the general population, because of the large numbers of false
positives and false negatives that occur with a lower AUC (i.e. people told
they are at high risk when they are not, or told they are at low risk when they
are not).

(8)Wallace HM (2009) Big tobacco and
the human genome: driving the scientific bandwagon? Genomics Society and
Policy, 5 (1), 80-133. On: http://www.hss.ed.ac.uk/genomics/documents/Vol5No1.pdf
. The tobacco industry also founded the science of genetics and behaviour by
claiming that likelihood of smoking is also determined by genetics: http://onlinelibrary.wiley.com/doi/10.1111/j.1360-0443.2010.02940.x/full
. Again, the genes that explain smoking behaviour (or indeed, any behaviour)
have largely failed to materialise. The idea that such genes should exist is
still based on the method of calculating 'heritability' devised by the
eugenicist Ronald Fisher in 1918. Fisher went on to work for the tobacco
industry in the 1950s.